Speak of the devil: Aphasia vs. delirium

Jim Siegler

Two weeks ago, I was called to the emergency room to see a patient who was confused. She was 71 years old, carried a history of hypertension and mild cognitive impairment, but was fully independent at baseline. She was brought in by her family because that evening she was not acting like herself. Her son, who she lives with, found her sitting alone in the study and staring at the wall. When he asked her if she was ok, she responded, “Oh, yeah, the wall needs new paint.” He escorted her to her bedroom, but when he asked if she was going to brush her teeth, she replied, “I’m just taking my time.” After a few more questions, it became obvious to him that she did not understand what he was asking her. So he brought her to the emergency room. Eventually, I was called to evaluate the patient to determine if this was delirium, or if it was aphasia.

But, before even getting into the differences between aphasia and delirium, why is this even important? Who cares?

The reason it’s important to recognize aphasia from delirium is because their causes and management are polar opposites. Aphasia is caused by a focal cortical lesion—like a stroke, tumor, or neurodegenerative syndrome. In contrast, delirium is caused by a systemic disturbance—like sepsis, hypoglycemia, or uremia—which causes global cerebral dysfunction.

So how does a neurologist approach this?

The first tip here is to figure out how to describe the features of a patient’s language. How is the patient’s language produced and understood? Are the words clearly enunciated (favoring aphasia) or slurred (favoring delirium)? Is the patient’s speech grammatically correct (delirium) or lacking in appropriate syntax (aphasia)? Is the patient’s prosody—or pattern of speech—fluent (delirium) or irregular (aphasia)? Can the patient understand spoken language (delirium) or is there a major difficulty with following simple verbal/written commands (aphasia)? Naming and repetition should also be assessed as part of any neurologic examination, but impairment in these modalities is not as useful in distinguishing delirium from aphasia.

What if the patient suddenly has difficulty following commands or the speech is nonsensical?

Is it delirium, or is it a receptive (sensory) aphasia? Recall that delirium is defined by its (1) fluctuating course and (2) inattention whereas aphasia lacks both of these features. In an acutely altered patient, the provider should identify whether the patient can maintain attention or not. This can be evaluated using a number of tasks that may rely on spoken language (assessing serial 7’s, spelling “WORLD” backward) or doesn’t (giving the patient a drawing task). The motor evaluation of inattention in a delirious patient involves testing for asterixis, either with arms and wrists fully extended or having the patient squeeze the fingers of the examiner (the “milk maid’s sign”). A delirious patient will struggle with these tasks, the extended hands may flap or the fingers may intermittently lose their grip. The aphasic patient, in contrast, may not have trouble with this.

Misery loves company.

Neurologic deficits don’t always occur in isolation. A keen examiner can often recognize more than one clue which would help him or her to localize the lesion. Consider language lateralization for this aspect. In nearly every right-handed patient, language localizes to the left cerebral hemisphere. I don’t always count on this for left-handed patients, where a quarter of patients are right hemisphere dominant or even have a more “distributed” language function. In knowing the patient’s handedness, the examiner might attend more closely to functions of neighboring brain regions in order to distinguish a focal neurologic deficit from a global cerebral impairment. That is the third pearl. For instance, in a right-hand dominant patient, one might really try to tease out a pronator drift of the right hand (signifying corticospinal tract injury), or relatively slower tapping of the right fingers or feet (also indicating subtle corticospinal tract dysfunction). In the left-handed patient, one might look for those subtle signs on either hemibody.

Back to our patient…

Regarding the 71-year-old woman I saw back in the emergency department, she was ultimately diagnosed with aphasia. Her words were clearly enunciated although her speech was not perfectly grammatically correct, and she made inappropriate comments to questions and commands—in keeping with the first clinical pearl. She was able to maintain attention well—the second pearl—and on further neurologic assessment, she had mild weakness in her right face and arm. The final pearl. A beautiful localization to the left posterior frontal and parietal lobes for all the neurologists out there.

And when you suspect a focal cortical lesion in the setting of presumed delirium, don’t be afraid to speak up. Your patient may not be able to.

I hope you enjoyed this special guest article! If you haven’t checked out Dr. Siegler’s site & podcast please check it out here. Both the site and podcast are packed with clinically useful information for neurologists and non-neurologists alike. Also, if you haven’t subscribed to this blog yet, you can do so by clicking here. You can also follow the site on Facebook and Twitter. Thanks for reading! Until next time, stay safe and treat aggressively!